Marijuana Poisoning

The plant Cannabis sativa has been used for centuries for the effects of its psychoactive resins. The term “marijuana” typically refers to tobacco-like preparations of the leaves and flowers. The plant contains more than 400 chemicals but the cannabinoid δ-9-tetrahydrocannabinol (THC) is the major psychoactive constituent. “Hashish” is the resin extracted from the tops of flowering plants and generally has a much higher THC concentration. Marijuana is the most commonly used illicit drug in the United States. Currently, several states have passed legislation to decriminalize possession of small amounts of marijuana for both medical and personal use and several other states have similar legislation under consideration. The most common form of marijuana use in humans is inhalation of the smoke of marijuana cigarettes, followed by ingestion. In animals, although secondhand smoke inhalation is possible, the most common source of exposure is through ingestion of the owner's marijuana supply. The minimum lethal oral dose for dogs for THC is more than 3 g/kg. Although the drug has a high margin of safety, deaths have been seen after ingestion of food products containing the more concentrated medical-grade THC butter. There are two specific cannabinoid receptors in humans and dogs, CB₁ (primarily in central nervous system) and CB₂ (peripheral tissues). In animals, following oral ingestion, clinical effects begin within 60 minutes. All of the neuropharmacologic mechanisms by which cannabinoids produce psychoactive effects have not been identified. However, CB₁ activity is believed to be responsible for the majority of cannabinoid clinical effects. Highly lipid soluble, THC is distributed in fat, liver, brain, and renal tissue. Fifteen percent of THC is excreted into the urine and the rest is eliminated in the feces through biliary excretion. Clinical signs of canine intoxication include depression, hypersalivation, mydriasis, hypermetria, vomiting, urinary incontinence, tremors, hypothermia, and bradycardia. Higher dosages may additionally cause nystagmus, agitation, tachypnea, tachycardia, ataxia, hyperexcitability, and seizures. Treatment of marijuana ingestion in animals is largely supportive. Vital signs including temperature and heart rate and rhythm must be continually monitored. Stomach content and urine can be tested for cannabinoids. Gas chromatography and mass spectrometry can be utilized for THC detection but usually may take several days and are not practical for initiation of therapy. Human urine drug-screening tests can be unreliable for confirmation of marijuana toxicosis in dogs owing to the interference of a large number of the metabolites in canine urine. False negatives may also arise if testing occurs too recently following THC ingestion. Thus, the use of human urine drug-screening tests in dogs remains controversial. No specific antidote presently exists for THC poisoning. Sedation with benzodiazepines may be necessary if dogs are severely agitated. Intravenous fluids may be employed to counter prolonged vomiting and to help control body temperature. Recently, the use of intralipid therapy to bind the highly lipophilic THC has been utilized to help reduce clinical signs. The majority of dogs experiencing intoxication after marijuana ingestion recover completely without sequellae. Differential diagnoses of canine THC toxicosis include human pharmaceuticals with central nervous system stimulatory effects, drugs with central nervous system depressant effects, macrolide parasiticides, xylitol, and hallucinogenic mushrooms.     

The Effect of Experimental Methyl Mercury Poisoning on the Distribution of Acid Phosphatase During Autolysis in Cat Liver

Seven healthy male cats weighing between 2.35 and 4.30 kg were daily fed a diet which contained Hg²⁰³ labelled methyl mercury hydroxide in liver homogenate. Eight additional cats were kept as controls on a similar diet without methyl mercury hydroxide. The daily amount of methyl mercury hydroxide fed to the cats, expressed as inorganic mercury, varied between 3.75 and 4.33 mg per cat. When the animals had developed neurological symptoms typical of methyl mercury poisoning, they were decapitated and their livers removed for the determination of the mercury content, the distribution of acid phosphatase during autolysis at 37°G, the pH and the total bacterial count before and after a 24 hr. period of autolysis. Similar determinations except for the mercury were made from the livers of the control animals. The total amount of methyl mercury hydroxide fed to the cats varied between 29.14 and 40.12 mg Hg++ per kg of body weight, and the mercury content in their livers between 102.5 and 128.7 mg Hg++ per kg of liver wet weight.The share of un sedimentable activity of acid phosphatase out of the total immediately after decapitation was found to be significantly (P < 0.001) greater in the livers of the methyl mercury-fed cats than in the livers of the control animals. After 12 to 24 hrs. of autolysis at 37 °G the unsedimentable activity accounted for 100 % of the total acid phosphatase activity in the livers of 6 of the 7 methyl mercury-fed animals, while in the livers of the controls the corresponding percentages varied after 24 hrs. of incubation between 42 and 73, the mean being 57.4 ± 11.4 %. The mean pH of the livers of the methyl mercury fed animals was found to be significantly higher before (P< 0.001) and after (P < 0.001) a 24 hr. incubation at 37 °G than the corresponding mean pH values of the control animals.Because of the injection of antibiotics given to the cats before sacrifice the total bacterial count of the livers, which was checked before and after a 24 hr. incubation at 37°G, was found to be zero.     

奶牛食盐中毒

食盐为奶牛重要的饲料成分之一，如采食过多或饲喂不当时，会发生中毒。现将我区某奶牛场发生的一起奶牛食盐中毒事故介绍如下：